Multi-site cardiac stimulation device and method for detecting retrograde conduction

ABSTRACT

An implantable cardiac stimulation device, such as a pacemaker, defibrillator and/or cardioverter, and an associated method that provide cardiac stimulation to at least two ventricular stimulation sites, within a single ventricle or across two ventricles. A high intrinsic atrial rate triggers a retrograde conduction detection routine when a high ventricular stimulation rate is sustained for a predetermined number of cycles during an atrial sensing mode. This routine interrupts concurrent stimulation, and alternates the stimulation output to the different ventricular sites.

PRIORITY CLAIM

This application is a continuation of U.S. patent application Ser. No.10/310,429, filed Dec. 4, 2002, now U.S. Pat. No. 6,862,477 titled“Multi-Site Cardiac Stimulation Device and Method for DetectingRetrograde Conduction,” which is a continuation of U.S. patentapplication Ser. No. 09/881,449, filed Jun. 13, 2001, now U.S. Pat. No.6,611,714, issued Aug. 26, 2003, which are incorporated herein byreference.

FIELD OF THE INVENTION

The present invention relates generally to programmable cardiacstimulating devices. More specifically, this is directed to amulti-chamber or biventricular cardiac stimulation device and associatedmethod for detecting retrograde conduction from one or more ventricularstimulation site for the purpose of identifying and terminatingpacemaker-mediated tachycardia (PMT).

BACKGROUND OF THE INVENTION

In a normal human heart, the sinus node, generally located near thejunction of the superior vena cava and the right atrium, constitutes theprimary natural pacemaker initiating rhythmic electrical excitation ofthe heart chambers. The cardiac impulse arising from the sinus node istransmitted to the two atrial chambers, causing a depolarization knownas a P-wave and the resulting atrial chamber contractions. Theexcitation pulse is further transmitted to and through the ventriclesvia the atrioventricular (A-V) node and a ventricular conduction systemcausing a depolarization known as an R-wave and the resultingventricular chamber contractions.

Disruption of this natural pacing and conduction system as a result ofaging or disease can be successfully treated by artificial cardiacpacing using implantable cardiac stimulation devices, includingpacemakers and implantable defibrillators, which deliver rhythmicelectrical pulses or other anti-arrhythmia therapies to the heart, viaelectrodes implanted in contact with the heart tissue, at a desiredenergy and rate. One or more heart chambers may be electricallystimulated depending on the location and severity of the conductiondisorder.

A single-chamber pacemaker delivers pacing pulses to one chamber of theheart, either one atrium or one ventricle. Dual chamber pacemakers arenow commonly available and can provide stimulation in both an atrialchamber and a ventricular chamber, typically the right atrium and theright ventricle. Both unipolar or bipolar dual chamber pacemakers existin which a unipolar or bipolar lead extends from an atrial channel ofthe dual chamber device to the desired atrium (e.g. the right atrium),and a separate unipolar or bipolar lead extends from a ventricularchannel to the corresponding ventricle (e.g. the right ventricle). Indual chamber, demand-type pacemakers, commonly referred to as DDDpacemakers, each atrial and ventricular channel includes a senseamplifier to detect cardiac activity in the respective chamber and anoutput circuit for delivering stimulation pulses to the respectivechamber.

If an intrinsic atrial depolarization signal (a P-wave) is not detectedby the atrial channel, a stimulating pulse will be delivered todepolarize the atrium and cause contraction. Following either a detectedP-wave or an atrial pacing pulse, the ventricular channel attempts todetect a depolarization signal in the ventricle, known as an R-wave. Ifno R-wave is detected within a defined atrial-ventricular interval (AVinterval, also referred to as AV delay), a stimulation pulse isdelivered to the ventricle to cause ventricular contraction. In thisway, atrioventricular synchrony is achieved by coordinating the deliveryof ventricular output in response to a sensed or paced atrial event.

Unfortunately, a pacemaker operating in the DDD mode may contribute, incombination with other factors, to a pacemaker-mediated tachycardia(PMT). For example, in patients who are prone to atrial arrhythmias,e.g., a fast atrial rate, the DDD pacer tracks the fast atrial rate,causing the ventricles to be paced at a correspondingly fast rate,thereby causing a tachycardia (fast heart rate) to occur. Without theDDD pacemaker, such tachycardia would probably not occur because theventricles would normally continue at a slower (more normal) rate,despite the fast atrial rate. However, with the DDD pacemaker, thestimulation of the ventricles occurs so as to track the fast atrialrate, and thus the pacemaker effectively intervenes or “mediates” so asto cause the tachycardia, appropriately termed a “pacemaker-mediatedtachycardia,” or PMT, to occur.

There are other reasons why a pacemaker-mediated tachycardia may betriggered by a DDD pacer, other than simply tracking a fast atrial rate.For example, prolonged intervals between atrial and ventriculardepolarization can cause or enhance retrograde conduction of thedepolarization wave back into the atria producing what is referred to asa “retrograde P-wave.” A retrograde P-wave may be sensed by the atrialchannel sensing circuits. Unfortunately, the pacemaker sensing circuitscannot differentiate between retrograde P-waves and normal P-waves, sosuch sensing may result in a pacemaker-mediated tachycardia wherein eachventricular paced event is followed by a retrograde P-wave which istracked, resulting in another ventricular paced event, causing theprocess to repeat.

It is well known that the type of pacemaker-mediated tachycardiadescribed above (resulting from sensing retrograde P-waves) can beprevented by programming the post ventricular atrial refractory period(PVARP) of the pacemaker to be longer than the retrograde conductiontime. Such lengthening of the PVARP, however, disadvantageously preventsthe sensing of a P-wave that occurs late in the PVARP. A failure tosense a P-wave, in turn, causes an atrial stimulus to be generated bythe pacemaker that is more than likely delivered into the heart's atrialrefractory period, at a time when such pulse is ineffective. Thisresults in an effective prolongation of the P-to-V interval, which mayeither decrease hemodynamic performance and/or induce retrogradeconduction. Even worse, the possibility exists that the atrial stimulus(delivered into the heart during the atrial refractory period) mayinduce atrial flutter or fibrillation.

Several approaches are known in the art to minimize the likelihood of apacemaker-mediated tachycardia caused by the sensing of retrogradeP-waves in patients having a dual-chamber pacing system. For example, amaximum tracking rate may be incorporated in modern DDD pacemakers.Another approach is Automatic Mode Switch that switches the pacing modefrom any tracking mode (DDD or VDD) to a non-tracking mode. If thenatural atrial rate exceeds this maximum tracking rate, the pacemakerconverts to a non-tracking mode (known as a DDI mode). Sensing continuesin both the atrium and the ventricle, but the ventricle is stimulated ata rate independent of the high atrial rate. If the atrial rate decreasesagain, the pacemaker may convert back to the DDD mode.

In order to detect pacemaker-mediated tachycardia, the time between theventricular stimulation pulse and a sensed P-wave may be measured. If ashort, stable interval is measured, the sensed P-wave is suspected ofbeing a retrograde P-wave. Corrective action may then be taken toterminate the pacemaker-mediated tachycardia, for example converting toan atrial non-tracking mode such as DDI.

Mounting clinical evidence supports the evolution of more complexcardiac stimulating devices capable of stimulating three or even allfour heart chambers to stabilize arrhythmias or to re-synchronize heartchamber contractions (Ref: Cazeau S., “Four chamber pacing in dilatedcardiomyopathy,” Pacing Clin. Electrophsyiol 1994 17(11 Pt 2):1974–9).Stimulation of multiple sites within a heart chamber has also been foundeffective in controlling arrhythmogenic depolarizations (Ref:Ramdat-Misier A., “Multisite or alternate site pacing for the preventionof atrial fibrillation,” Am. J. Cardiol., 1999 11;83(5b):237D–240D). Inthese multi-site or multi-chamber stimulation applications, correctsynchronization of all heart chambers is vital to achieving a desiredhemodynamic benefit. However, the occurrence of retrograde P-wavesduring biventricular or multi-site ventricular stimulation may lead topacemaker-mediated tachycardia in the same way as described for dualchamber pacemakers. Retrograde P-waves may arise from more than oneventricular stimulation site. Therefore, in multi-site and multi-chamberstimulation devices, detection of retrograde P-waves and prevention ofpacemaker-mediated tachycardia is just as important as in dual chamberdevices.

The ability to detect the presence of retrograde P-waves duringstimulation of more than one site within the ventricles, however,becomes more complex than in dual chamber stimulation because theretrograde P-waves may be arising from more than one retrograde pathway,each with a different conduction time. Sensed retrograde P-waves willincrease the detected atrial rate indicating an atrial tachycardia whenin fact there is none causing the stimulation device to deliver orwithhold stimulation inappropriately. Sensed retrograde P-waves may alsoinduce pacemaker-mediated tachycardia. Both of these situations arehighly undesirable. What is needed, therefore, is a method for detectingretrograde P-waves during biventricular or multi-site ventricularstimulation and determining the site of ventricular stimulationassociated with the retrograde conduction.

SUMMARY

The present invention addresses this need by providing an implantablecardiac stimulation device capable of stimulating at two or moreventricular sites and possessing a retrograde conduction detectionalgorithm. The retrograde conduction detection algorithm is executedwhenever a pacemaker-mediated tachycardia is suspected.

The retrograde conduction detection algorithm (or routine) detects thepresence of two or more retrograde conduction pathways arising from twoor more ventricular stimulation sites. The retrograde conductiondetection algorithm will effectively terminate a pacemaker-mediatedtachycardia due to the presence of one retrograde conduction pathway. Iftwo retrograde conduction pathways are identified, automatic adjustmentof the stimulation device operating parameters is made to terminate thepacemaker-mediated tachycardia and prevent inappropriate arrhythmiadetection.

The present invention provides an implantable cardiac stimulation deviceequipped with cardiac data acquisition capabilities. A preferredembodiment of the stimulation device includes a control system forcontrolling the operation of the device; a set of leads for receivingcardiac signals and for delivering atrial and ventricular stimulationpulses; a set of sensing circuits comprised of sense amplifiers forsensing and amplifying the cardiac signals; a sampler, such as an A/Dconverter for sampling cardiac signals; and pulse generators forgenerating atrial and ventricular stimulation pulses. In addition, thestimulation device includes a memory for storing operational parametersfor the control system, such as cardiac signal sampling parameters andtiming intervals such as AV and PV delays, and measured cardiac signalintervals. The device also includes a telemetry circuit forcommunicating with an external programmer.

When operating according to a preferred embodiment, the retrogradeconduction detection algorithm sets the PV delays for each ventricularstimulation site to temporary test settings that are not equal to eachother. Ventricular stimulation is delivered in an alternating fashion tothe ventricular stimulation sites. If only one retrograde path exists,alternating the stimulation will effectively terminate apacemaker-mediated tachycardia.

To detect if two retrograde conduction pathways exist, the mean intervalfrom a ventricular stimulation pulse to the subsequent sensed P-wave (VPinterval) is measured for each stimulation site. The standard deviationsof the mean VP intervals for each ventricular stimulation site are thencompared to a minimum acceptable value. If the standard deviation issmall, retrograde conduction is detected for the correspondingventricular stimulation site.

Retrograde conduction from two or more sites is further confirmed by amathematical relationship examining the change in atrial rate relativeto the change in VP intervals. If retrograde conduction is confirmed fortwo or more pathways, automatic adjustment of operating parameters,preferably an extension of the post-ventricular atrial blanking period,is made to terminate the pacemaker-mediated tachycardia. Adjustments arealso made to prevent inappropriate arrhythmia detection due to thepacemaker-mediated tachycardia.

The stimulation device measures the time delay between the pacing of aventricular site to the sensed P-wave in the corresponding atrium. Thestandard deviations of these retrograde conduction times for eachventricular sites are used to derive VP interval stability for differentretrograde paths. The study of the relationship between averageretrograde conduction stability and atrial heart rate within a fewcardiac cycles confirms and identifies the source(s) of other retrogradeconduction paths in existence. The identification of the retrogradepaths enhances the response of the stimulation device to terminate aPMT, and helps qualify the atrial rate information used by thecardioverter to discriminate supraventricular tachyarrhythmia fromventricular tachyarrhythmia.

The system and method of the present invention thus provide a method fordetecting retrograde conduction pathways arising from more than oneventricular stimulation site. The present invention further provides asafe, effective method of terminating pacemaker-mediated tachycardia dueto retrograde conduction arising from one or more ventricularstimulation sites. By appropriately detecting a pacemaker-mediatedtachycardia due to retrograde conduction, accurate arrhythmia detectionfor the purposes of cardioversion or shocking therapy is also improved.

BRIEF DESCRIPTION OF THE DRAWINGS

Further features and advantages of the present invention may be morereadily understood by reference to the following description taken inconjunction with the accompanying drawings, in which:

FIG. 1 is a simplified, partly cutaway view illustrating an implantablestimulation device in electrical communication with at least three leadsimplanted into a patient's heart for delivering multi-chamberstimulation and shock therapy;

FIG. 2 is a functional block diagram of the multi-chamber implantablestimulation device of FIG. 1, illustrating the basic elements thatprovide pacing stimulation, cardioversion, and defibrillation in fourchambers of the heart;

FIG. 3 is a flow chart providing an overview of the operations includedin the present invention for responding to a high atrial rate in thedevice of FIG. 2;

FIG. 4 is a flow chart depicting the method used in the operations ofFIG. 3 for determining if a sensed high atrial rate is caused byretrograde conduction; and

FIG. 5 is a timing diagram illustrating a sequence of atrial andventricular events occurring during the retrograde conduction detectionalgorithm of FIG. 4.

DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS

The following description is of a best mode presently contemplated forpracticing the invention. This description is not to be taken in alimiting sense but is made merely for the purpose of describing thegeneral principles of the invention. The scope of the invention shouldbe ascertained with reference to the issued claims. In the descriptionof the invention that follows, like numerals or reference designatorswill be used to refer to like parts or elements throughout. The presentinvention is directed at detecting retrograde conduction in animplantable cardiac stimulating device possessing pacing, cardioversionand defibrillation capabilities. A general cardiac stimulation devicewill thus be described in conjunction with FIGS. 1 and 2, in which theretrograde conduction detection feature of the present invention couldbe implemented. It is recognized, however, that numerous variations ofsuch a device exist in which the methods of the present invention couldbe implemented without deviating from the scope of the presentinvention.

FIG. 1 illustrates a stimulation device 10 in electrical communicationwith a patient's heart 12 by way of three leads 20, 24 and 30 suitablefor delivering multi-chamber stimulation and shock therapy. To senseatrial cardiac signals and to provide right atrial chamber stimulationtherapy, the stimulation device 10 is coupled to an implantable rightatrial lead 20 having at least an atrial tip electrode 22, whichtypically is implanted in the patient's right atrial appendage. Theright atrial lead 20 may also have an atrial ring electrode 23 to allowbipolar stimulation or sensing in combination with the atrial tipelectrode 22.

To sense the left atrial and ventricular cardiac signals and to provideleft-chamber stimulation therapy, the stimulation device 10 is coupledto a “coronary sinus” lead 24 designed for placement in the “coronarysinus region” via the coronary sinus ostium so as to place a distalelectrode adjacent to the left ventricle and additional electrode(s)adjacent to the left atrium. As used herein, the phrase “coronary sinusregion” refers to the vasculature of the left ventricle, including anyportion of the coronary sinus, great cardiac vein, left marginal vein,left posterior ventricular vein, middle cardiac vein, and/or smallcardiac vein or any other cardiac vein accessible by the coronary sinus.

Accordingly, the coronary sinus lead 24 is designed to receive atrialand ventricular cardiac signals and to deliver: left ventricular pacingtherapy using at least a left ventricular tip electrode 26, left atrialpacing therapy using at least a left atrial ring electrode 27, andshocking therapy using at least a left atrial coil electrode 28. In analternative embodiment, the coronary sinus lead 24 may also include aleft ventricular ring electrode 25.

For a more detailed description of a coronary sinus lead, reference ismade, for example, to U.S. Pat. No. 5,466,254, titled “Coronary SinusLead with Atrial Sensing Capability” (Helland).

The stimulation device 10 is also shown in electrical communication withthe patient's heart 12 by way of an implantable right ventricular lead30 having, in this embodiment, a right ventricular tip electrode 32, aright ventricular ring electrode 34, a right ventricular (RV) coilelectrode 36, and an SVC coil electrode 38. Typically, the rightventricular lead 30 is transvenously inserted into the heart 12 so as toplace the right ventricular tip electrode 32 in the right ventricularapex so that the RV coil electrode 36 will be positioned in the rightventricle and the SVC coil electrode 38 will be positioned in thesuperior vena cava. Accordingly, the right ventricular lead 30 iscapable of receiving cardiac signals, and delivering stimulation in theform of pacing and shock therapy to the right ventricle.

FIG. 2 illustrates a simplified block diagram of the multi-chamberimplantable stimulation device 10, which is capable of treating bothfast and slow arrhythmias with stimulation therapy, includingcardioversion, defibrillation, and pacing stimulation. While aparticular multi-chamber device is shown, this is for illustrationpurposes only, and one of skill in the art could readily duplicate,eliminate or disable the appropriate circuitry in any desiredcombination to provide a device capable of treating the appropriatechamber(s) with cardioversion, defibrillation and pacing stimulation.

The stimulation device 10 includes a housing 40 which is often referredto as “can”, “case” or “case electrode”, and which may be programmablyselected to act as the return electrode for all “unipolar” modes. Thehousing 40 may further be used as a return electrode alone or incombination with one or more of the coil electrodes 28, 36, or 38, forshocking purposes. The housing 40 further includes a connector having aplurality of terminals 42, 43, 44, 46, 48, 52, 54, 56, and 58 (shownschematically and, for convenience, the names of the electrodes to whichthey are connected are shown next to the corresponding terminals). Assuch, to achieve right atrial sensing and stimulation, the connectorincludes at least a right atrial tip terminal (A_(R) TIP) 42 adapted forconnection to the atrial tip electrode 22. The connector may alsoinclude a right atrial ring terminal (A_(R) RING) 43 for connection tothe atrial ring electrode 23.

To achieve left chamber sensing, pacing, and shocking, the connectorincludes at least a left ventricular tip terminal (V_(L) TIP) 44, a leftatrial ring terminal (A_(L) RING) 46, and a left atrial shocking coilterminal (A_(L) COIL) 48, which are adapted for connection to the leftventricular tip electrode 26, the left atrial ring electrode 27, and theleft atrial coil electrode 28, respectively.

To support right ventricular sensing, pacing and shocking, the connectorfurther includes a right ventricular tip terminal (V_(R) TIP) 52, aright ventricular ring terminal (V_(R) RING) 54, a right ventricularshocking coil terminal (RV COIL) 56, and an SVC shocking coil terminal(SVC COIL) 58, which are adapted for connection to the right ventriculartip electrode 32, right ventricular ring electrode 34, the RV coilelectrode 36, and the SVC coil electrode 38, respectively.

At the core of the stimulation device 10 is a programmablemicrocontroller 60 that controls the various modes of stimulationtherapy. As is well known in the art, the microcontroller 60 typicallyincludes a microprocessor, or equivalent control circuitry, designedspecifically for controlling the delivery of stimulation therapy, andmay further include RAM or ROM memory, logic and timing circuitry, statemachine circuitry, and I/O circuitry. Typically, the microcontroller 60includes the ability to process or monitor input signals (data) ascontrolled by a program code stored in a designated block of memory. Thedetails of the design and operation of the microcontroller 60 are notcritical to the present invention. Rather, any suitable microcontroller60 may be used that carries out the functions described herein. The useof microprocessor-based control circuits for performing timing and dataanalysis functions are well known in the art.

Representative types of control circuitry that may be used with thepresent invention include the microprocessor-based control system ofU.S. Pat. No. 4,940,052 (Mann et al.). For a more detailed descriptionof the various timing intervals used within the stimulation device andtheir inter-relationship, reference is made to U.S. Pat. No. 4,788,980(Mann et al.).

FIG. 2 illustrates an atrial pulse generator 70 and a ventricular pulsegenerator 72 that generate stimulation pulses for delivery by the rightatrial lead 20, the right ventricular lead 30, and/or the coronary sinuslead 24 via an electrode configuration switch 74. It is understood thatin order to provide stimulation therapy in each of the four chambers ofthe heart, the atrial and ventricular pulse generators, 70 and 72, mayinclude dedicated, independent pulse generators, multiplexed pulsegenerators, or shared pulse generators. The atrial pulse generator 70and the ventricular pulse generator 72 are controlled by themicrocontroller 60 via appropriate control signals 76 and 78,respectively, to trigger or inhibit the stimulation pulses.

The microcontroller 60 further includes timing control circuitry 79which is used to control the timing of such stimulation pulses (e.g.pacing rate, atrio-ventricular (AV) delay, atrial interconduction (A-A)delay, or ventricular interconduction (V-V) delay, etc.), as well as tokeep track of the timing of refractory periods, blanking intervals,noise detection windows, evoked response windows, alert intervals,marker channel timing, etc., which is well known in the art.

The switch 74 includes a plurality of switches for connecting thedesired electrodes to the appropriate I/O circuits, thereby providingcomplete electrode programmability. Accordingly, the switch 74, inresponse to a control signal 80 from the microcontroller 60, determinesthe polarity of the stimulation pulses (e.g. unipolar, bipolar,cross-chamber, etc.) by selectively closing the appropriate combinationof switches (not shown) as is known in the art.

Atrial sensing circuits (ATR. SENSE) 82 and ventricular sensing circuits(VTR. SENSE) 84 may also be selectively coupled to the right atrial lead20, coronary sinus lead 24, and the right ventricular lead 30, throughthe switch 74, for detecting the presence of cardiac activity in each ofthe four chambers of the heart. Accordingly, the atrial and ventricularsensing circuits 82 and 84 may include dedicated sense amplifiers,multiplexed amplifiers, or shared amplifiers. The switch 74 determinesthe “sensing polarity” of the cardiac signal by selectively closing theappropriate switches. In this way, the clinician may program the sensingpolarity independent of the stimulation polarity.

Stimulation during pacing can be performed in a bipolar mode in devicescombining pacing and cardioversion/defibrillation functions becauseunipolar stimulation may interfere with arrhythmia detection. Hence, inone embodiment of the present invention, the switch bank 74 isconfigured such that: right atrial pacing and sensing is performed in abipolar fashion between the right atrial tip electrode 22 and rightatrial ring electrode 23; right ventricular pacing and sensing isperformed in a bipolar fashion between right ventricular tip electrode32 and right ventricular ring electrode 34; and left ventricular pacingand sensing is performed in a bipolar fashion between coronary sinus tipelectrode 26 and the coronary sinus ring electrode 27. Right ventricularsensing may alternatively be configured between the right ventricularcoil electrode 36 and the right ventricular ring electrode 34. Bipolarsensing may also be achieved using an integrated bipolar lead whereinthe right ventricular coil electrode 36 and right ventricular ringelectrode 34 are electrically coupled within the right ventricular leadbody 30. Bipolar sensing is then performed between the right ventriculartip electrode 32 and the coupled right ventricular coil electrode 36 andright ventricular ring electrode 34. The electrode combinations used forpacing and sensing are not critical to the present invention. Rather,any electrode combination that allows acceptable stimulation and sensingthresholds may be used. By employing the right ventricular coilelectrode 36, possibly in combination with right ventricular ringelectrode 34, the electrode surface during sensing is increased,advantageously reducing the effects of lead polarization. Othertechniques of reducing lead polarization such as titanium nitridecoating may also be used to improve the operation of the presentinvention. Each sensing circuit, 82 and 84, preferably employs one ormore low power, precision amplifiers with programmable gain andautomatic gain or sensitivity control, bandpass filtering, and athreshold detection circuit, to selectively sense the cardiac signal ofinterest. The automatic sensitivity control enables the stimulationdevice 10 to deal effectively with the difficult problem of sensing thelow amplitude signal characteristics of atrial or ventricularfibrillation. For a more detailed description of a sensing circuit,reference is made to U.S. Pat. No. 5,573,550, titled “ImplantableStimulation Device having a Low Noise, Low Power, Precision Amplifierfor Amplifying Cardiac Signals” (Zadeh et al.). For a more detaileddescription of an automatic sensitivity control system, reference ismade to U.S. Pat. No. 5,685,315, titled “Cardiac Arrhythmia DetectionSystem for an Implantable Stimulation Device” (McClure et al.).

The outputs of the atrial and ventricular sensing circuits, 82 and 84,are connected to the microcontroller 60 for triggering or inhibiting theatrial and ventricular pulse generators 70 and 72, respectively, in ademand fashion, in response to the absence or presence of cardiacactivity in the appropriate chambers of the heart. The atrial andventricular sensing circuits 82 and 84, in turn, receive control signalsover signal lines 86 and 88 from the microcontroller 60, for controllingthe gain, threshold, polarization charge removal circuitry (not shown),and the timing of any blocking circuitry (not shown) coupled to theinputs of the atrial and ventricular sensing circuits 82 and 84.

For arrhythmia detection, the stimulation device 10 utilizes the atrialand ventricular sensing circuits 82 and 84 to sense cardiac signals fordetermining whether a rhythm is physiologic or pathologic. As usedherein “sensing” is reserved for the noting of an electrical signal, and“detection” is the processing of these sensed signals and noting thepresence of an arrhythmia. The timing intervals between sensed events(e.g. P-waves, R-waves, and depolarization signals associated withfibrillation which are sometimes referred to as “F-waves” or“Fib-waves”) are then classified by the microcontroller 60 by comparingthem to a predefined rate zone limit (e.g. bradycardia, normal, low rateVT, high rate VT, and fibrillation rate zones) and various othercharacteristics (e.g. sudden onset, stability, physiologic sensors, andmorphology, etc.), in order to determine the type of remedial therapythat is needed (e.g. bradycardia pacing, anti-tachycardia stimulation,cardioversion shocks or defibrillation shocks, collectively referred toas “tiered therapy”). Discrimination algorithms may be employed in orderto distinguish supraventricular tachycardia from ventriculartachycardia.

Cardiac signals are also applied to the inputs of a data acquisitionsystem 90, which is depicted as an analog-to-digital (A/D) converter forsimplicity of illustration. The data acquisition system 90 is configuredto acquire intracardiac electrogram (EGM) signals, convert the rawanalog data into digital signals, and store the digital signals forlater processing and/or telemetric transmission to an external device102. The data acquisition system 90 is coupled to the right atrial lead20, the coronary sinus lead 24, and the right ventricular lead 30through the switch 74 to sample cardiac signals across any pair ofdesired electrodes.

Advantageously, the data acquisition system 90 may be coupled to themicrocontroller 60 or another detection circuitry, for detecting anevoked response from the heart 12 in response to an applied stimulus,thereby aiding in the detection of “capture”. Capture occurs when anelectrical stimulus applied to the heart is of sufficient energy todepolarize the cardiac tissue, thereby causing the heart muscle tocontract. The microcontroller 60 detects a depolarization signal duringa window following a stimulation pulse, the presence of which indicatesthat capture has occurred. The microcontroller 60 enables capturedetection by triggering the ventricular pulse generator 72 to generate astimulation pulse, starting a capture detection window using the timingcontrol circuitry 79 within the microcontroller 60, and enabling thedata acquisition system 90 via control signal 92 to sample the cardiacsignal that falls in the capture detection window and, based on theamplitude, determines if capture has occurred.

Capture detection may occur on a beat-by-beat basis or on a sampledbasis. Preferably, a capture threshold search is performed once a dayduring at least the acute phase (e.g., the first 30 days) and lessfrequently thereafter. A capture threshold search would begin at adesired starting point (either a high energy level or the level at whichcapture is currently occurring) the energy level would be decreaseduntil capture is lost. The lowest value at which capture still occurs isknown as the capture threshold. Thereafter, a working margin is added tothe capture threshold. The implementation of capture detection circuitryand algorithms are well known.

The microcontroller 60 is further coupled to a memory 94 by a suitabledata/address bus 96, wherein the programmable operating parameters usedby the microcontroller 60 are stored and modified, as required, in orderto customize the operation of the stimulation device 10 to suit theneeds of a particular patient. Such operating parameters define, forexample, stimulation pulse amplitude, pulse duration, electrodepolarity, rate, sensitivity, automatic features, arrhythmia detectioncriteria, and the amplitude, waveshape and vector of each stimulationpulse to be delivered to the patient's heart 12 within each respectivetier of therapy. A feature of the present invention is the ability tosense and store a relatively large amount of data (e.g., from the dataacquisition system 90), which data may then be used for subsequentanalysis to guide the programming of the device. According to themethods included in the present invention, data will be collected andstored in memory to be analyzed for the detection of retrogradeconduction. The results of this analysis are used for programming device10 operating parameters for terminating a pacemaker-mediatedtachycardia.

Advantageously, the operating parameters of the stimulation device 10may be non-invasively programmed into the memory 94 through a telemetrycircuit 100 in telemetric communication with the external device 102,such as a programmer, transtelephonic transceiver, or a diagnosticsystem analyzer. The telemetry circuit 100 is activated by themicrocontroller 60 by a control signal 106. The telemetry circuit 100advantageously allows intracardiac electrograms and status informationrelating to the operation of the stimulation device 10 (as contained inthe microcontroller 60 or memory 94) to be sent to the external device102 through the established communication link 104.

The stimulation device 10 may further include a physiologic sensor 108,commonly referred to as a “rate-responsive” sensor because it istypically used to adjust stimulation rate according to the exercisestate of the patient. However, the physiological sensor 108 may furtherbe used to detect changes in cardiac output, changes in thephysiological condition of the heart, or diurnal changes in activity(e.g. detecting sleep and wake states). Accordingly, the microcontroller60 responds by adjusting the various stimulation parameters (such asrate, AV Delay, V-V Delay, etc.) at which the atrial and ventricularpulse generators 70 and 72 generate stimulation pulses.

The stimulation device 10 additionally includes a power source such as abattery 110 that provides operating power to all the circuits shown inFIG. 2. For the stimulation device 10, which employs shocking therapy,the battery 110 must be capable of operating at low current drains forlong periods of time, preferably less than 10 μA, and also be capable ofproviding high-current pulses when the patient requires a shock pulse,preferably, in excess of 2 A, at voltages above 2 V, for periods of 10seconds or more. The battery 110 preferably has a predictable dischargecharacteristic so that elective replacement time can be detected.Accordingly, the stimulation device 10 can employ lithium/silvervanadium oxide batteries.

As further illustrated in FIG. 2, the stimulation device 10 is shown toinclude an impedance measuring circuit 112 that is enabled by themicrocontroller 60 by means of a control signal 114.

It is a function of the stimulation device 10 to operate as animplantable cardioverter/defibrillator (ICD) device. That is, it mustdetect the occurrence of an arrhythmia, and automatically apply anappropriate electrical stimulation or shock therapy to the heart aimedat terminating the detected arrhythmia. To this end, the microcontroller60 further controls a shocking circuit 116 by way of a control signal118. The shocking circuit 116 generates shocking pulses of low (up to0.5 Joules), moderate (0.5–10 Joules), or high (11 to 40 Joules) energy,as controlled by the microcontroller 60. Such shocking pulses areapplied to the patient's heart through at least two shocking electrodes,and as shown in this embodiment, selected from the left atrial coilelectrode 28, the RV coil electrode 36, and/or the SVC coil electrode 38(FIG. 1). As noted above, the housing 40 may act as an active electrodein combination with the RV coil electrode 36, or as part of a splitelectrical vector using the SVC coil electrode 38 or the left atrialcoil electrode 28 (i.e., using the RV coil electrode 36 as a commonelectrode).

Cardioversion shocks are generally considered to be of low to moderateenergy level (so as to minimize pain felt by the patient), and/orsynchronized with an R-wave and pertaining to the treatment oftachycardia. Defibrillation shocks are generally of moderate to highenergy level (i.e., corresponding to thresholds in the range of 5–40Joules), delivered asynchronously (since R-waves may be toodisorganized), and pertaining exclusively to the treatment offibrillation. Accordingly, the microcontroller 60 is capable ofcontrolling the synchronous or asynchronous delivery of the shockingpulses.

In FIG. 3, a flow chart is shown describing an overview of the operationand novel features implemented in one embodiment of the device 10. Inthis flow chart, and the other flow charts described herein, the variousalgorithmic steps are summarized in individual “blocks”. Such blocksdescribe specific actions or decisions that must be made or carried outas the algorithm proceeds. Where a microcontroller (or equivalent) isemployed, the flow charts presented herein provide the basis for a“control program” that may be used by such a microcontroller (orequivalent) to effectuate the desired control of the stimulation device.Those skilled in the art may readily write such a control program basedon the flow charts and other descriptions presented herein.

FIG. 3 shows that initially the device 10 is operating normally in theprogrammed mode for delivering stimulation therapy at step 305. If atany time during the normal stimulation mode, a pacemaker-mediatedtachycardia is suspected, as determined at decision step 310, aretrograde conduction detection algorithm is executed at step 400. Theretrograde conduction detection algorithm will be described in detail inconjunction with FIG. 4. The criteria used at decision step 310 fordetermining when a pacemaker-mediated tachycardia is suspected arepredefined. For example, if the ventricular stimulation rate exceeds adefined rate limit during atrial sensing for a given number ofconsecutive cardiac cycles, pacemaker-mediated tachycardia is suspected.If the ventricular stimulation rate remains high after the retrogradeconduction detection algorithm, the device 10 automatically switches toa non-tracking mode at step 320. In some cases, pacemaker-mediatedtachycardia will be terminated during the execution of the retrogradeconduction detection algorithm 400. In such cases the device 10 mayimmediately return to the normal stimulation mode 305.

The retrograde conduction detection algorithm 400 is shown in FIG. 4.The algorithm begins at step 405 wherein the PV delays corresponding toeach ventricular stimulation site are adjusted to predefined test PVdelay settings. The PV delay for the first stimulation site, referred toas PV₁, is set to a different value than the PV delay for the secondstimulation site, referred to as PV₂. For example, the PV₁ delay may beset to 150 msec, and the PV₂ delay may be set to 130 msec. Ventricularstimulation is then delivered to each stimulation site in an alternatingfashion at step 410: on the first cycle stimulation is delivered to thefirst stimulation site after a PV₁ delay, and, on the subsequent cardiaccycle, stimulation is delivered to the second stimulation site after aPV₂ delay.

If only one retrograde pathway is present, alternating the delivery ofstimulation between the two stimulation sites will terminate apacemaker-mediated tachycardia. For example, if retrograde conduction isarising from the second ventricular stimulation site, stimulation atonly the first ventricular stimulation site on one cardiac cycle willstop the retrograde conduction from arising from the second site forthat cycle. This will allow the naturally occurring P-wave to be sensedduring the subsequent cycle. If no intrinsic P-wave is detected, anatrial stimulation pulse will be delivered. Thus, the retrogradeconduction detection algorithm 400 will effectively terminate apacemaker-mediated tachycardia due to retrograde conduction arising fromone ventricular stimulation site.

The ventricular stimulation pulses are delivered in an alternate fashionfor a predefined number of cardiac cycles, e.g. eight cardiac cycles, atstep 410. The intervals from each ventricular stimulation pulse to thesubsequent P-wave, hereafter referred to as a “VP interval,” aremeasured at step 415. At step 420 the mean VP intervals are determined.All VP intervals associated with the first ventricular stimulation siteare averaged to determine a mean V₁P interval. All VP intervalsassociated with the second ventricular stimulation site are averaged todetermine a mean V₂P interval.

The standard deviation of the mean V₁P interval and the standarddeviation of the mean V₂P interval are then calculated at step 425. Ifretrograde conduction is present, the standard deviations of the mean VPintervals are expected to be small because retrograde conduction time isexpected to be constant. The standard deviations are compared to aminimum value at step 430. If the standard deviations are less than theminimum value, two retrograde conduction paths are detected for thecorresponding stimulation sites. If only one retrograde conductionpathway was present, a pacemaker-mediated tachycardia will have beenterminated in the first two alternating stimulation cycles, therefore noretrograde conduction will be found.

If the standard deviations are not less than the predefined minimum,then no retrograde conduction is detected. The algorithm 400 returns tostep 315 of FIG. 3. If high rate ventricular stimulation is stilloccurring, the operating mode is switched to a non-tracking mode. It ispresumed that the high ventricular rate is associated with a highintrinsic atrial rate. If the high ventricular stimulation ratecontinues during atrial sensing (PV mode), the retrograde conductiondetection algorithm will be repeated after a predefined number of PVcycles. If the intrinsic atrial rate remains persistently high, theprogrammed maximum tracking rate will limit the ventricular stimulationrate.

The standard deviation of the VP interval is one indication of thepresence of retrograde conduction, however, the change in atrial ratewith respect to a corresponding VP interval should also be examined toverify retrograde conduction. Changes in the ventricular rate due to anactivity sensor-indicated rate or a maximum tracking rate can causevariations in the PV interval of one heart cycle that subsequentlyaffects the following VP interval. Thus appropriate variations in the PVinterval due to ventricular-based timing in a DDD stimulation mode couldresult in small variation of the VP interval without the presence ofretrograde conduction. Thus, if retrograde conduction was identified atstep 430 of FIG. 4 according to the minimum standard deviation criteria,the existence of two retrograde conduction paths is further confirmed atdecision step 435 by calculating the following relation between theatrial intervals and the VP intervals:If |P ₂ P ₃ −P ₁ P ₂|−2×|meanV ₁ P−meanV ₂ P|<X, then two retrogradepaths,  (1)where

-   -   P₂P₃ represents the time interval from the second atrial sensed        P-wave to the third atrial sensed P-wave;    -   P₁P₂ represents the time interval from the first atrial sensed        P-wave to the second atrial sensed P-wave;    -   MeanV₁P represents the mean of the V₁P interval;    -   MeanV₂P represents the mean of the V₂P interval; and    -   X represents a predefined programmable tolerance in        milliseconds, preferably on the order of 20 msec.

If the difference between the two atrial sensed cycle intervals is lessthan a predefined amount greater than twice the difference between thetwo mean VP intervals, two retrograde conduction paths exist. Equation(1) is the difference between the following two equations:P ₁ P ₂=Ventricular Rate−V ₁ P+V ₂ P  (2)P ₂ P ₃=Ventricular Rate−V ₂ P+V ₁ P  (3)Thus the change in the atrial rate from the first PV cycle to the secondPV cycle (P₂P₃−P₁P₂) is compare to the change in the VP intervals. Ifthe change in the atrial rate less the change in the VP intervals isless than a predefined tolerance, then two retrograde conduction pathsare confirmed at step 435.

If the relation of Equation (1) is not true, then one or no retrogradeconduction exists. If only one retrograde conduction path was present,the retrograde conduction detection algorithm will have successfullyterminated the pacemaker-mediated tachycardia by alternating ventricularstimulation sites. If the atrial rate changes account for the smallvariation in VP intervals, then no retrograde conduction can beconfirmed. Therefore device 10 may return to its normal operating mode,step 305 (FIG. 3).

The timing diagram shown in FIG. 5 illustrates the relationship of thetiming intervals used in the calculation of Equation (1). On the atrialchannel 501, three consecutive P-waves are shown, P₁, P₂, and P₃, 506,508, 510, respectively. The first atrial P-wave, P₁ 506, is followed bythe PV₁ delay 512 and a ventricular stimulation pulse, V₁ 520 (shown onthe ventricular channel 502), which is delivered to a first ventricularstimulation site. The second atrial P-wave, P₂ 508, is followed by a PV₂delay 514 and a ventricular stimulation pulse V₂ 522, which is deliveredto a second ventricular stimulation site. In this example, the PV₁ delay512 is set to 150 msec, and the PV₂ delay 514 is set to 130 msec. Thecalculation according to equation 1 for the example intervals shown inFIG. 5 is:|430−470|−2×|320−300|=40−40=0

Therefore, in this example, retrograde conduction is occurring from bothventricular stimulation sites since the relationship between the changein the atrial rate and the change in the VP intervals does not exceedthe minimum allowed tolerance.

As shown in FIG. 4, if two retrograde conduction paths are confirmed atstep 435, then automatic adjustment of device 10 operating parameters ismade to terminate the pacemaker-mediated tachycardia at step 440. In apreferred embodiment, if device 10 is a multi-chamber pacemaker, thepost-ventricular atrial refractory period (referred to as PVARP) isextended. Preferably, PVARP is adjusted to be greater than the longer ofthe two retrograde conduction times, i.e. longer than the greatest meanVP interval. In this way, a retrograde conducted P-wave will occurduring the PVARP and not be tracked for ventricular stimulationpurposes. Instead, the next intrinsic atrial P-wave occurring after theextended PVARP will be sensed or an atrial stimulation pulse will bedelivered thus terminating the pacemaker-mediated tachycardia.

If device 10 is also a cardioverter defibrillator and retrogradeconduction is detected, the detected atrial rate interval is ignored atstep 445 if the algorithm for discriminating between supraventriculartachycardia and ventricular tachycardia is enabled. In this way, theretrograde conduction is not inappropriately detected as asupraventricular tachycardia potentially triggering inappropriatetherapy delivery. Having detected both retrograde conduction pathwaysand taken appropriate action for terminating a pacemaker-mediatedtachycardia, device 10 may now return to the normal operating mode 305(FIG. 3)

Thus, a system and method for detecting retrograde conduction from oneor more ventricular stimulation sites during biventricular or multi-siteventricular stimulation. By identifying which ventricular stimulationsites are associated with a retrograde conduction pathway, appropriateaction can be taken to terminate a pacemaker-mediated tachycardia.Furthermore, confirmation and termination of a pacemaker-mediatedtachycardia will prevent an inappropriate arrhythmia detection andinappropriate cardioversion or shock therapy from being delivered. Whilethe present invention has been described according to specificembodiments, this description is intended for illustration and notlimitation. Those skilled in the art may modify features or methodsdescribed herein without departing from the scope of the presentinvention.

1. In an implantable cardiac stimulation device, a method comprising:delivering stimulation energy to at least two ventricular sites duringnormal cardiac cycles; detecting that a potential pacemaker-mediatedtachycardia condition exists; measuring VP intervals for the at leasttwo ventricular sites; determining respective measures of variabilityfor the respective VP intervals; comparing the measures of variabilitywith a threshold value, and determining that retrograde conductionexists for each ventricular site if the measures of variability fallbelow the threshold; wherein determining a measure of variabilitycomprises determining a standard deviation for the VP intervalscorresponding to each ventricular site.
 2. The method of claim 1,further comprising determining that no retrograde conduction exists ifthe measures of variability exceed the threshold.
 3. The method of claim1, wherein upon confirming retrograde conduction for the at least twoventricular sites, automatically adjusting an operating parameter. 4.The method of claim 3, wherein automatically adjusting an operatingparameter comprises extending a post-ventricular atrial blanking period.5. An implantable cardiac stimulation device comprising: a pulsegenerator that is operative to generate pacing pulses; a lead systemconfigured to deliver the pacing pulses to at least two ventricularsites; a sensor system that is configured to detect atrial activity andoperative to generate corresponding signals; and a controller connectedto the sensor system and operative to process the signals to measure VPintervals for the at least two ventricular sites and determinerespective measures of variability for the respective VP intervals,wherein the controller is further operative to compare the measures ofvariability with a threshold value, and to determine that retrogradeconduction exists for each ventricular site if the measures ofvariability fall below the threshold; wherein the controller isoperative to determine a measure of variability by determining astandard deviation for the VP intervals corresponding to eachventricular site.
 6. The implantable cardiac stimulation device of claim5, wherein the controller is operative to determine that no retrogradeconduction exists if the measures of variability exceed the thresholdvalue.
 7. The implantable cardiac stimulation device of claim 5, whereinthe controller is responsive to determining retrograde conduction forthe at least two ventricular sites to automatically adjust an operatingparameter.
 8. The implantable cardiac stimulation device of claim 7,wherein the controller is operative to extend a post-ventricular atrialblanking period.
 9. In a biventricular implantable cardiac stimulationdevice, a method comprising: delivering stimulation energy to a rightventricle and a left ventricle during normal cardiac cycles; detectingthat a potential pacemaker-mediated tachycardia condition exists,measuring at least three VP intervals for the right ventricle and theleft ventricle; determining respective measures of variability for therespective at least three VP intervals; comparing the measures ofvariability with a threshold value, and determining that retrogradeconduction exists for each of the ventricles if the measures ofvariability fall below the threshold.
 10. The method of claim 9, furthercomprising determining that no retrograde conduction exists if themeasures of variability exceed the threshold.
 11. The method of claim 9,wherein determining a measure of variability comprises determining astandard deviation for the at least three VP intervals corresponding toright ventricle and the left ventricle.
 12. The method of claim 9,wherein upon confirming retrograde conduction for the right ventricleand the left ventricle, automatically adjusting an operating parameter.13. The method of claim 12, wherein automatically adjusting an operatingparameter comprises extending a post-ventricular atrial blanking period.14. A biventricular implantable cardiac stimulation device comprising: apulse generator that is operative to generate pacing pulses; a leadsystem configured to deliver the pacing pulses to a right ventricle anda left ventricle; a sensor system that is configured to detect atrialactivity and operative to generate corresponding signals; and acontroller connected to the sensor system and operative to process thesignals to measure at least three VP intervals for the right ventricleand the left ventricle and determine respective measures of variabilityfor the respective at least three VP intervals, wherein the controlleris further operative to compare the measures of variability with athreshold value, and to determine that retrograde conduction exists foreach ventricular site if the measures of variability fall below thethreshold.
 15. The biventricular implantable cardiac stimulation deviceof claim 14, wherein the controller is operative to determine that noretrograde conduction exists if the measures of variability exceed thethreshold value.
 16. The biventricular implantable cardiac stimulationdevice of claim 14, wherein the controller is operative to determine ameasure of variability by determining a standard deviation for the atleast three VP intervals corresponding to each ventricle.
 17. Thebiventricular implantable cardiac stimulation device of claim 14,wherein the controller is responsive to determining retrogradeconduction for right ventricle and the left to automatically adjust anoperating parameter.
 18. The biventricular implantable cardiacstimulation device of claim 17, wherein the controller is operative toextend a post-ventricular atrial blanking period.